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Many people around the world are actively contributing to expanding the science of Oilahuasca. It has not been perfected yet. What's presented here works very well for some individuals. However, countless tests have shown that there are individuals who simply cannot get effects from any allylbenzenes no matter which set of known activators they use. The exact reason for this is currently unknown. We are still searching for Oilahuasca activation formulas that will work for more people.

For 24 hours prior to using oilahuasca you must follow the Oilahuasca Diet restrictions.

For a list of herbal formulas, supplements, and dietary restrictions known to be effective in obtaining psychedelic effects from allylbenzenes please see the article Oilahuasca Activators.

THIS PAGE EXPLAINS THE OILAHUASCA THEORY. MANY FACTS ARE PRESENTED TO SUPPORT THE OILAHUASCA THEORY. HOWEVER ALL SECTIONS ON THIS PAGE SHOULD BE TREATED AS THEORETICAL UNLESS STATED AS FACT.

THIS IS A WORK IN PROGRESS. IT WILL BE UPDATED AS NEW DATA IS AVAILABLE. TO LEAVE FEEDBACK FOR THIS PAGE USE THE DISCUSS LINK AT THE BOTTOM OF THIS ARTICLE.

THE FACTS BEHIND OILAHUASCA

Herbs containing allylbenzenes, such as nutmeg, can produce psychedelic effects under certain circumstances. This is well documented.

Several allylbenzenes have been proven to form up to 3 alkaloid metabolites after ingestion by several animals.[2][3] They do not form amphetamines in vivo as has been speculated in the past. The alkaloids detected in animal urine are tertiary aminopropiophenones of 3 possible subtypes: dimethylamines, piperidines, and pyrrolidines.[1][2][3][4]

The allylbenzene elemicin has been proven to form all 3 different alkaloid metabolites after ingestion in animals by analyzing urine using gas-liquid chromatography and chemical ionization mass spectrometry.[1]

Safrole is also proven to form all three alkaloid metabolites after ingestion.[2]

Myristicin appears to only form piperidines and pyrrolidines. Dimethylamines of myristicin have not been detected.[3]

Allylbenzene, from which all allylbenzenes are derived, forms piperidine and dimethylamine alkaloids.[4]

Propenylbenzene and its derivatives (asarone, anethole, etc.) do not form alkaloid metabolites.[4]

While it is a fact that allylbenzenes do form alkaloids in vivo, just how this occurs is currently unknown. The current facts show that allylbenzenes first form 1'-hydroxy metabolites, and then these form 1'-oxo metabolites. The 1'-oxo metabolites probably then condense with endogenous amines in vivo without enzymatic activity. The 1'-oxo metabolite 1'-oxosafrole of the allylbenzene safrole, for example, is proven to form alkaloid adducts by simply mixing it together at room temperature with endogenous amines such as dimethylamine, piperidine, and pyrrolidine without the need for enzymatic action.[8][9] This is probably the route by which these alkaloids occurs in vivo, but this is not yet proven.

The oilahuasca theory attempts to explain this process, and appears to work using enzyme inhibitors and inducers which are shown to help coerce the human body into creating allylbenzene alkaloid metabolites in vivo.

BASIC OILAHUASCA THEORY

The oilahuasca activation theory was originally put together by 69ron with the help of many other active forum members of herbs.maxforum.org and www.drugs-forum.com who also took part in most of the human tests done which have shown the oilahuasca activation theory appears to be a working model. The theory is still evolving as new information arrives. The current theory incorporates some elements that originated from Oswald and Peele's activation theory, as well as research by many other individuals.

Many enzymes are present in humans which cause allylbenzenes to form inactive metabolites. In some people these inactive metabolites far out number the active ones, leading to little or no activity. While in others their digestive systems consistently form the active alkaloid metabolites in abundance, leading to psychoactivity.

Compounds that help activate these allylbenzenes are collectively referred to as oilahuasca activators. In essence these activators work by inhibiting enzymes which prevent activation while inducing enzymes that help activation.

Once the allylbenzenes are in their 1'-hydroxylated alcohol form, they are vulnerable to attack by UGT and SULT, so these must be inhibited so that they can then be converted to phenyl vinyl ketones by the action of 17bHSD2. If they are in their 3'-hydroxylated form they can still probably be attacked by UGT and SULT, so these should probably be inhibited so that they can be turned into aldehydes by a currently unknown enzyme action (probably also the action of 17bHSD2).

SEQUENCE A (based on work by Oswald)

NEW EVIDENCE IS SHOWING PROBLEMS IN THE SEQUENCE A THEORY

Sequence B (based on work from the Oilahuasca pioneers) appears to have more evidence to support it than Sequence A (based on work by Oswald) in humans. Unlike Sequence A, one of the alkaloid metabolites in Sequence B is proven to occur in humans. The 3 end alkaloid metabolites in the Sequence A theory are only proven to be created in animals in vivo. There is of yet no evidence to suggest that they occur in humans.

Metabolites from steps 1-3 are proven steps to occur. How Sequence A is supposed to go from step 3 to step 4 is currently unknown. And no supporting evidence has yet been found for this to happen in humans.

Over the past few years, an overwhelming amount of test results seem to indicate that Sequence A probably does not work in humans. Human Oilahuasca tests seem to point in the direction of Sequence B being the more likely activation sequence.

SEQUENCE A - STEP 3: CONVERSION TO A PHENYL VINYL KETONE

SEQUENCE A - STEP 4: CONVERSION TO ALKALOIDS

The alkaloids that form in this section have been detected in vivo. But how exactly they form from 1'-oxoelemicin is unknown. A transaminase enzyme may be required, or 1'-oxoelemicin might condense spontaneously to form alkaloids.

Of the possible alkaloid metabolites, the dimethylamine form has the lowest lipid solubility and the piperidine form has the highest lipid solubility. Therefore, the piperidine alkaloid form will more easily cross the blood brain barrier.

At this time it is not known which of the possible alkaloid metabolites might be the main active metabolite for each of the allylbenzenes. Other amines may also form.

It’s important to note that in the case of the allylbenzene myristicin, piperidine and pyrrolidine metabolites have been detected but dimethylamine metabolites have not. This indicates that the dimethylamine metabolites might possibly be more vulnerable to attack by enzymes such as MAO-A, MAO-B, etc., leading to their complete destruction prior to being excreted in urine.

Sequence B appears to have more evidence to support it than Sequence A in humans. Unlike Sequence A, one of the alkaloid metabolites in Sequence B is proven to occur in humans. Some of the alkaloid metabolites theoretically created by Sequence A have only been found in some animals so far.

Please note that steps 1-3 are proven to occur for some allylbenzenes such as methyl eugenol. Step 4 is a proven alkaloid metabolite for methyl chavicol (see the article 4-Methoxycinnamoylglycine for more details). These sequences will lead to similar alkaloids as produced in Sequence A. In Sequence A the step before alkaloid creation is a ketone. Ketones tend not to form adducts as easily as aldehydes. Because step 3 is an aldehyde in Sequence B, this greatly increases the likelihood of alkaloids forming in vivo. Many aldehydes such as cinnamaldehyde are proven to form adducts with amino acids and other amines very easily without the need for a catalyst. See the article Cinnamaldehyde for more details on aldehyde adducts.

For activation Sequence B, it's important to inhibit the 1'-hydroxylation pathway. This is theorized to be a route to inactivation. Enzymes known to cause 1'-hydroxylation include CYP1A2, CYP2A6, and CYP2C9.

A proposed alternate glycine adduct is {(Z)-[(2E)-3-(3,4,5-trimethoxyphenyl)prop-2-en-1-ylidene]amino}acetic acid. Cinnamaldehyde is known to create a similar adduct with potassium glycine. See the Cinnamaldehyde article for more details.

OILAHUASCA ACTIVATION VIA ENZYME MANIPULATION

This section details all the known enzymes to induce and inhibit in order to optimize the psychedelic and/or stimulant actions various allylbenzenes are capable of producing when fully activated. In some people allylbenzenes are extremely difficult to activate. Failure to follow these guidelines completely can lead to little or no effects from the various allylbenzenes available.

There are several subsets of glutathione S-transferase (GST). The exact ones responsible for this action are currently unknown, as is there level of interaction in this adduct process. Inhibitors must be used. For information on inhibitors see the article here: Glutathione S-transferase.

TRANSDERMAL USE VERSUS ORAL USE

THIS SECTION IS BASED ON ANECDOTAL DATA ONLY

Tests performed by several individuals have shown that topical application of these allylbenzenes can produce effects that are 5-10 times stronger than that of oral use. When used topically, the onset of the effects are also quicker and the overall duration of the effects are shortened as well. With topical use there are also less side effects.[5]

ALLYLBENZENE POLLS

After hundreds of votes have been made, the allylbenzene polls have consistently shown the same results year after year. As of May 2015, a total of 689 votes have been collected for the 2 polls. The results show very clearly that one of the three oils is by far the most effective in most people. It's interesting to note however, that the votes are not unanimous. The fact that the least effective essential oil is also the most effective essential oil for a minority of the people polled, shows just how different people are in how they are affected by these essential oils.

The nutmeg poll found in the article Nutmeg gives very strong evidence that the Oilahuasca theory is correct, which states that the allylbenzenes must be activated in the body before they can become psychedelic. If they were psychedelic without needing activation, they would be psychedelic in everyone all the time, but they clearly are not. The nutmeg poll results have been running for several years and the results are the same year after year. They show that most people find nutmeg to be psychedelic sometimes. However, not everyone does. A large minority finds nutmeg is never psychedelic.

The difficulty of activating elemicin, methyl chavicol, or myristicin varies from person to person. Some people can only easily activate one of these and have great difficulty trying to activate the others. Few people are able to easily activate all three. Many people have difficulty even activating just one of these. Hopefully, in the future, the Oilahuasca theory will advance enough to change this reality, making all three easy to activate in all people. Right now, that is not the case.

One major problem in advancing the Oilahuasca theory is finding people who are unable to get any hallucinogenic effects from allylbenzenes who are also willing to take part in the study. These people, because they don't initially get any results, are usually skeptics and right it all off as nonsense and aren't willing to further advance the Oilahuasca techniques. This is unfortunate. These are the very people who need to help advance the Oilahuasca theory. Their bodies are especially resistant to Oilahuasca techniques. If the reason for this resistance could be determined, it could greatly advance the Oilahuasca techniques for everyone. Currently, most of the individuals working on advancing Oilahuasca techniques are people who are already occasionally getting it to work.

To view the results of these polls, you need to cast your vote.

These polls are live polls hosted by www.pollsnack.com and are 100% anonymous. You don't need to log in to vote.

ALLYLBENZENE P450 ENZYME SPECIFICS

NOTE: This section refers to the actions of fully activated allylbenzenes via oilahuasca activation. For example, eugenol fully activated is a stimulant, but when not fully activated its a sedative (as is the case for most allylbenzenes when not fully activated).

OILAHUASCA DIET

For 24 hours prior to using oilahuasca you must follow the Oilahuasca Diet restrictions.

Human diet is a major factor in getting oilahuasca working. Many people consume food, drinks and supplements known to inhibit 17bHSD2. Drinks as commonplace as tea and grapefruit juice potently inhibit 17bHSD2. These and other detrimental dietary items explained in this article must be avoided for at least 24 hours prior to using oilahuasca if psychedelic effects are desired. Failure to adhere to these dietary guidelines can completely prevent oilahuasca from working. The 17bHSD2 enzyme is critical for oilahuasca to work. If this enzyme is inhibited by drinking tea or ingesting similar 17bHSD2 inhibitors, it can be impossible to get oilahuasca working. This has been verified by several people. Please adhere to these diet guidelines if you want any success with oilahuasca.

SUPPLEMENTS AND FOODS TO AVOID

All inhibitors of oxidative 17bHSD2 will prevent activation of allylbenzenes. This enzyme must be induced, not inhibited. It's the single most important enzyme to induce. If oxidative 17bHSD2 is not functioning, allylbenzenes cannot produce psychedelic activity.[5]

It's not known which metabolites of the allylbenzenes are the preferred alkaloid metabolites. Avoid these substances if you specifically want to avoid making too many dimethylamine metabolites.

Anecdotal reports indicate that supplementation with piperidine sources improves activation, and supplementation with dimethylamine sources reduces psychedelic activity. The exact reason for this is currently unknown. Some reports indicate that methyl eugenol and myristicin can be inactive in some cases unless used with piperidine supplements.

BENEFICIAL SUPPLEMENTS

Berberine is one of the most powerful activators tested. It potently inhibits CYP2D6, and inhibits CYP2C9 and CYP3A4, while leaving CYP2E1 active. There may be other unknown actions at play. When used with caffeine (inhibits CYP1A2) and steviosides (theorized to inhibit UGT2B7), it's been able to activate elemicin at doses smaller than any other activator tested. It works better than black pepper tea, and produces a cleaner experience. Black pepper has sedative effects in the doses used, and colors up the experience.

It's believed that berberine's lack of sedative effects and it's potent inhibition of CYP2D6 and it's inaction on CYP2E1 are why it's more effective than black pepper. CYP2D6 appears to be extremely detrimental to activation and CYP2E1 appears to be vital. Piperine found in black pepper has been shown to inhibit CYP2E1[19] to some degree in humans, which is not good.

Note that black pepper contains piperine and other alkaloids in addition to piperidine. Piperine inhibits CYP3A4 which is good, but it also has some other actions, such as inhibiting CYP2E1[19] to some degree, which is not good. More tests need to be performed on isolated piperine to determine it's effectiveness. When making black pepper tea, filtering out the solids removes a lot of the piperine. Piperine’s solubility in water is only 9.4 mg per cup. However, piperine is potent, and 10-20 mg of piperine can inhibit CYP3A4. 5 grams of black pepper contains about 500 mg of piperine, but only 9.4 mg will be extracted into 1 cup of water. The rest remains in the solid black pepper grounds. 1 cup of water can hold all the piperidine in black pepper.

Genistein induces 17bHSD2, an essential enzyme required for activation. It also inhibits UGT, SULT, and GST. Genistein is still being researched. It's effectiveness has been called into question. Until more data is available, it might be better to avoid genistein. Kudzu, from which it is extracted, was found to reduce psychedelic action by interacting with 5-HT1A, 5-HT2A, and 5-HT2C receptors.

See the articles Genistein and 17bHSD2 for more details and references to the facts stated above.

Glycerol

Acts as an SSAO inhibitor. When using glucosamine to inhibit SSAO it's probably best use it 1 hour before and then again combined with coffee at the time the allylbenzenes are ingested, and a few times periodically throughout the experience to boost the psychedelic effects. Doses of 1500 mg glucosamine HCl have been tested along with coffee producing very good results. Its possible that lower doses are effective but they have not been tested. Glucosamine has a half life of approximately 15 hours. It's SSAO inhibition is likely to last at least 15 hours or more.

See the articles Glucosamine and SSAO for more details and references to the facts stated above.

It can take 3 or more hours for food to reach the colon (this varies dramatically from person to person, and depends highly on other contents in the digestive system). For this reason L-lysine supplements should be take several hours before taking allylbenzenes.